Dear reader,

I am a first year university student and i just wrote a midterm for my human physiology course. A question that appeared on the midterm was:

Action potentials occur at the:

A) axon 
B) dendrites
C) soma (cell body)
D) a), b), and c)

I answered D (a, b, and c) but my professor says that is incorresct and the write answer is A.

From studying for the midterm i read that if an action potential occurs midway down the axon an action potential propogates down towards the axon terminal aswell as up towards the cell body and dendrites. I also know that the cell body and dentrites of a neuron have voltage gated ion channels in their membranes and can therefore support the conductance of an action potential.

My professors argument is that naturally occuring action potentials only originate at the axon hillock and therefore only travel in one direction, which is down the axon. So, in order for an action potential to originate at the axon it would have to be done experimentally.

Based on the wording of the question i find my choice (d) to be more suitable. Yes, A (axon) is correct, however; D (a, b, and c) is more correct.

What do you think?

Rule number one: your professor is always right,
Rule number two: when your professor is wrong, rule number one applies.

In this case I agree with your professor - naturally ocurring APs start in the axon initial segment (very close to the soma). For more information see a very recent paper:-

Nature Neuroscience 11, 178 - 186 (2008)
Published online: 20 January 2008 | doi:10.1038/nn2040


Action potential generation requires a high sodium channel density in the axon initial segment
Maarten H P Kole1, Susanne U Ilschner1, Björn M Kampa1,4, Stephen R Williams1,2, Peter C Ruben1,3 & Greg J Stuart1


--------------------------------------------------------------------------------

The axon initial segment (AIS) is a specialized region in neurons where action potentials are initiated. It is commonly assumed that this process requires a high density of voltage-gated sodium (Na+) channels. Paradoxically, the results of patch-clamp studies suggest that the Na+ channel density at the AIS is similar to that at the soma and proximal dendrites. Here we provide data obtained by antibody staining, whole-cell voltage-clamp and Na+ imaging, together with modeling, which indicate that the Na+ channel density at the AIS of cortical pyramidal neurons is 50 times that in the proximal dendrites. Anchoring of Na+ channels to the cytoskeleton can explain this discrepancy, as disruption of the actin cytoskeleton increased the Na+ current measured in patches from the AIS. Computational models required a high Na+ channel density (2,500 pS m-2) at the AIS to account for observations on action potential generation and backpropagation. In conclusion, action potential generation requires a high Na+ channel density at the AIS, which is maintained by tight anchoring to the actin cytoskeleton.